Duick D S, Stein R B, Warren D W, Nicoloff J T
J Clin Endocrinol Metab. 1975 Aug;41(2):229-34. doi: 10.1210/jcem-41-2-229.
Recent evidence indicates that triiodothyronine (T3) administration may not completely inhibit normal thyroid secretion. To further corroborate this observation, measurement of serum T4-RIA concentrations was performed on 15 normal controls (10 men, 5 women; ages 20-42) who were placed on 100 mug of T3 daily for a 5-week period. Decrements of 53%, 36%, and 28% from the baseline T4-RIA were noted at weeks 1, 2, and 3 respectively. At 3 weeks a nadir T4-RIA of 2.5 mug/100 ml was reached which did not significantly differ from the 4th (2.9 mug/100 ml) and 5th weeks (2.6 mug/100 ml). Further, seven euthyroid patients who had received replacement thyroid hormone for 1-16 were switched to T3 (75-100 mug/day) for 28 days. At the end of this period, their mean T4-RIA was 2.6 mug/100 ml. Similar T3 treatment studies were performed on 20 primary hypothyroid patients. After 4 weeks of T3 all 20 patients displayed a T4-RIA below the limits of assay detectability (less than 0.625 mug/100 ml) while all euthyroid subjects had values greater than 1.2 mug/100 ml. Suppression of T4-RIA with T3 was also noted in 4 patients with pituitary and 2 patients with hypothalamic hypothyroidism. Three days after cessation of T3 treatment in normal subjects, no significant rise in mean T4-RIA was seen (2.3 mug/100 ml). Subsequently, T4-RIA rose to 4.5 mug/100 ml on day 7 and 6.7 mug/100 ml on day 10 (74% of the presuppression value) in normals. A similar rise to 7.9 mug/100 ml 10 days after withdrawal from T3 was noted in the euthyroid subjects who had received long-term thyroid hormone replacement. In contrast, all primary hypothyroid patients had either a minimal or nondetectable elevation in T4-RIA while demonstrating a marked rise in TSH 10 days after T3 withdrawal. An absent or impaired rise in T4-RIA after T3 withdrawal was also noted in patients with pituitary and hypothalamic hypothyroidism. These observations indicated: 1) There is continued thyroidal T4 secretion in euthyroid subjects receiving 100 mug of T3 daily. 2) The hypothesis is advanced that an intact hypothalamic-pituitary-tyhroid axis may be required for continued T4 secretion while on T3. 3) The duration of prior suppression with thyroid hormone medication does not appear to influence this phenomenon.
近期证据表明，给予三碘甲状腺原氨酸（T3）可能无法完全抑制正常甲状腺分泌。为进一步证实这一观察结果，对15名正常对照者（10名男性，5名女性；年龄20 - 42岁）进行了血清T4 - RIA浓度测定，这些对照者连续5周每日服用100微克T3。在第1、2和3周时，T4 - RIA分别较基线水平下降了53%、36%和28%。在第3周时，T4 - RIA达到最低点，为2.5微克/100毫升，与第4周（2.9微克/100毫升）和第5周（2.6微克/100毫升）无显著差异。此外，7名接受甲状腺激素替代治疗1 - 16年的甲状腺功能正常患者改用T3（75 - 100微克/天）治疗28天。在此期间结束时，他们的平均T4 - RIA为2.6微克/100毫升。对20名原发性甲状腺功能减退患者进行了类似的T3治疗研究。T3治疗4周后，所有20名患者的T4 - RIA均低于检测限（低于0.625微克/100毫升），而所有甲状腺功能正常的受试者的值均大于1.2微克/100毫升。在4名垂体性甲状腺功能减退患者和2名下丘脑性甲状腺功能减退患者中也观察到T3对T4 - RIA的抑制作用。正常受试者停止T3治疗3天后，平均T4 - RIA未见显著升高（2.3微克/100毫升）。随后，正常受试者在第7天T4 - RIA升至4.5微克/100毫升，第10天升至6.7微克/100毫升（为抑制前值的74%）。接受长期甲状腺激素替代治疗的甲状腺功能正常受试者在停用T3 10天后，T4 - RIA也有类似升高，达到7.9微克/100毫升。相比之下，所有原发性甲状腺功能减退患者在T4 - RIA方面仅有轻微升高或未检测到升高，而在停用T3 10天后促甲状腺激素（TSH）显著升高。垂体性和下丘脑性甲状腺功能减退患者在停用T3后也出现T4 - RIA升高缺失或受损的情况。这些观察结果表明：1）每日接受100微克T3治疗的甲状腺功能正常受试者甲状腺仍持续分泌T4。2）提出假说，即甲状腺功能正常受试者在服用T3期间持续分泌T4可能需要完整的下丘脑 - 垂体 - 甲状腺轴。3）先前甲状腺激素药物抑制的持续时间似乎不影响这一现象。
